| First Author | Katoh A | Year | 2007 |
| Journal | J Neurophysiol | Volume | 97 |
| Issue | 2 | Pages | 1280-7 |
| PubMed ID | 17005620 | Mgi Jnum | J:135841 |
| Mgi Id | MGI:3794668 | Doi | 10.1152/jn.00322.2006 |
| Citation | Katoh A, et al. (2007) Motor deficits in homozygous and heterozygous p/q-type calcium channel mutants. J Neurophysiol 97(2):1280-7 |
| abstractText | P/Q-type voltage-dependent Ca(2+) channels (VDCCs) are highly expressed in the cerebellum, and mutations of these channels are associated with disrupted motor function. Several allelic variants of the alpha1A pore-forming subunit of P/Q-type VDCCs have been described, and mice homozygous for these mutations exhibit gait ataxia, as do alpha1A knockout mice. Here we report that heterozygous alpha1A mutants also have a motor phenotype. Mice heterozygous for the leaner and alpha1A knockout mutations exhibit impaired motor learning in the vestibulo-ocular reflex (VOR), suggesting that subtle disruption of P/Q Ca(2+) currents is sufficient to disrupt motor function. Basal VOR and optokinetic reflex performance were normal in the heterozygotes but severely impaired in the leaner and alpha1A knockout homozygotes. |
